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The role of TNFa in mice exposed to radiation
https://repo.qst.go.jp/records/69329
https://repo.qst.go.jp/records/69329fc75406f-4448-4db9-8191-8e6afb99d665
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2008-04-28 | |||||
| タイトル | ||||||
| タイトル | The role of TNFa in mice exposed to radiation | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Hachiya, Misao
× Hachiya, Misao× Sibata, Tomohiro× Miyamura, Taichi× Akashi, Makoto× 蜂谷 みさを× 柴田 知容× 宮村 太一× 明石 真言 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Exposure to high dose radiation results in radiation injury which is a serious problem in accidental exposure and also in radiation therapy. There are many reports that radiation activates the production of tumor necrosis factor a (TNFa) in various cells including monocytes/macrophages and granulocytes. TNFa is well known as a pro-inflammatory cytokine and this factor plays a critical role in the initiation and continuation of inflammation and immunity. The excess production of TNFa leads to damage of tissues and organs. Previous studies showed that pretreatment with TNFa protected lethally radiated mice from death. On the other hand, there also are repots that radiation induced apoptosis through TNFa production. Thus, the role(s) of TNFa is not fully understood in radiation exposure. In this study, we investigated the roles of TNFa in mice exposed to radiation. We compared the wild-type (TNFa +/+) and the knockout (TNFa-/-) BALB/c mice. Both mice were subjected to g-ray radiation at doses of 6 -10 Gy. The survival durations in TNFa+/+ mice were significantly longer than those in TNFa-/- mice. We compared numbers of blood cells, numbers of surviving intestinal crypts, apoptosis in crypt cells and activity of an antioxidant enzyme manganese superoxide dismutase (MnSOD) in various organs following radiation. There was no significant difference in numbers of white blood cells after exposure. Furthermore, there was also no significant difference in surviving intestinal crypts after exposure and apoptosis in crypt cells between TNFa+/+and TNFa -/- mice. On day 15 after exposure, however, numbers of red blood cells in TNFa+/+ mice was higher than those in TNFa-/- mice. Activities of MnSOD were lower in liver of TNFa-/- than that of TNFa+/+mice. We also studied the expression of apoptosis-related proteins in mouse intestinal epithelial cells along the crypt-villus axis after radiation. Epithelial cells were sequentially isolated cells from the villus tip to the crypts of mouse small intestine by the modified Weiser method. The Bcl2 protein was constitutively expressed and its level was reduced by radiation in TNFa+/+ mice. In contrast, Bcl2 was not expressed in TNFa-/- mice and radiation did not induce Bcl2 expression. Since administration of TNFa prior to radiation has been shown to have radio-protective effect in mice, our results suggest that TNFa endogenously produced may play important roles in the radiation-induced injuries. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | ＡＡＣＲ Ａｎｎｕａｌ Ｍｅｅｔｉｎｇ 2008 | |||||
| 発表年月日 | ||||||
| 日付 | 2008-04-16 | |||||
| 日付タイプ | Issued | |||||
